Investigating the role of cnd-1 in C. elegans neuromuscular development
Disciplines
Cell Biology | Developmental Biology | Molecular and Cellular Neuroscience | Molecular Genetics
Abstract (300 words maximum)
Disorders such as autism and schizophrenia have been on the rise during the 21st century. A gene that has been linked to these disorders is NeuroD, which codes for a transcription factor that helps control cell fate in the early development of neuron and pancreatic cells. Caenorhabditis elegans, a species of nematode, has a simple and easily observable nervous system with genes homologous to humans. This makes them a prime candidate for research into human neurodevelopmental disorders. Previous research revealed that cnd-1, the homologous transcription factor to NeuroD, was found to control the expression of ceh-5, a Vax2-like homeobox class transcription factor, in RME head motoneurons and PVQ interneurons. cnd-1 functions with the Hox gene ceh-13 in defining the fate of DD-class embryonic ventral nerve cord motorneurons. However, it is unclear how body wall muscles interact with DD neurons, how cnd-1 plays a role in that process, and the implications this could have for certain neuromuscular dysfunctions. To address this research gap, we designed an approach to create a C. elegans strain containing both the cnd-1 mutation and genetically encoded fluorescent body wall muscle markers. The strain RSL85 contains an unc-27::GFP (green fluorescent protein) that is expressed in the body wall muscles. Our study aims to cross unc-27::GFP with our cnd-1 mutant and observe muscle cell morphology in comparison to our control unc-27::GFP strain. We expect to see differences in neuromuscular connectivity, which may explain the uncoordinated movement seen in cnd-1 mutants.
Academic department under which the project should be listed
CSM - Molecular and Cellular Biology
Primary Investigator (PI) Name
Dr. Martin Hudson
Investigating the role of cnd-1 in C. elegans neuromuscular development
Disorders such as autism and schizophrenia have been on the rise during the 21st century. A gene that has been linked to these disorders is NeuroD, which codes for a transcription factor that helps control cell fate in the early development of neuron and pancreatic cells. Caenorhabditis elegans, a species of nematode, has a simple and easily observable nervous system with genes homologous to humans. This makes them a prime candidate for research into human neurodevelopmental disorders. Previous research revealed that cnd-1, the homologous transcription factor to NeuroD, was found to control the expression of ceh-5, a Vax2-like homeobox class transcription factor, in RME head motoneurons and PVQ interneurons. cnd-1 functions with the Hox gene ceh-13 in defining the fate of DD-class embryonic ventral nerve cord motorneurons. However, it is unclear how body wall muscles interact with DD neurons, how cnd-1 plays a role in that process, and the implications this could have for certain neuromuscular dysfunctions. To address this research gap, we designed an approach to create a C. elegans strain containing both the cnd-1 mutation and genetically encoded fluorescent body wall muscle markers. The strain RSL85 contains an unc-27::GFP (green fluorescent protein) that is expressed in the body wall muscles. Our study aims to cross unc-27::GFP with our cnd-1 mutant and observe muscle cell morphology in comparison to our control unc-27::GFP strain. We expect to see differences in neuromuscular connectivity, which may explain the uncoordinated movement seen in cnd-1 mutants.